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Distribution and localization patterns of estrogen receptor-beta and insulin-like growth factor-1 receptors in neurons and glial cells of the female rat substantia nigra: localization of ERbeta and IGF-1R in substantia nigra
Quesada A, Romeo HE, Micevych P.. The Journal of comparative neurology, 2007-07-01
Topic: Brain proteins, microglia and lab models
Although several studies have focused on the neuroprotective effects of estrogen (E2) on stroke, there have been tantalizing reports on the potential neuroprotective role of E2 in degenerative neuronal diseases such as Alzheimer's and Parkinson's (PD). In animal models of PD, E2 protects the nigrostriatal dopaminergic (DA) system against neurotoxins. However, little is known about the cellular and molecular mechanism(s) involved by which E2 elicits its neuroprotective effects on the nigrostriatal DA system. A preferred mechanism for neuroprotection is the interaction of E2 with specific neuroprotective growth factors and receptors. One such neuroprotective factor/receptor system is insulin-like growth factor-1 (IGF-1). E2 neuroprotective effects in the substantia nigra (SN) DA system have been shown to be dependent on IGF-1. To determine whether E2 also interacts with the IGF-1 receptor (IGF-1R) and to determine the cellular localization of estrogen receptor (ER) and IGF-1R, we compared the distribution of ER and IGF-1R in the SN. Stereological measurements revealed that 40% of the subpopulation of tyrosine hydroxylase-immunoreactive (TH-ir) SN pars compacta (SNpc) DA neurons are immunoreactive for estrogen receptor-beta (ERbeta). No immunolabeling for ERalpha was observed. In situ hybridization and immunocytochemistry studies confirmed the expression of IGF-1R mRNA and revealed that almost all TH-ir SNpc DA neurons were immunoreactive for IGF-1R, respectively. Moreover, one-third of glial fibrillary acidic protein (GFAP-ir) cells in the SN were ERbeta-ir, and 67% of GFAP-ir cells expressed IGF-1R-ir. Therefore, the localization of ERbeta and IGF-1R on SNpc DA neurons and astrocytes suggests a modulatory role of E2 on IGF-1R, and this modulation may affect neuroprotection.
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APA 7th
Quesada, A., Romeo, H. E., & Micevych, P. (2007). Distribution and localization patterns of estrogen receptor-beta and insulin-like growth factor-1 receptors in neurons and glial cells of the female rat substantia nigra: localization of ERbeta and IGF-1R in substantia nigra. The Journal of comparative neurology. https://doi.org/10.1002/cne.21358
Vancouver
Quesada A, Romeo HE, Micevych P. Distribution and localization patterns of estrogen receptor-beta and insulin-like growth factor-1 receptors in neurons and glial cells of the female rat substantia nigra: localization of ERbeta and IGF-1R in substantia nigra. The Journal of comparative neurology. 2007. doi:10.1002/cne.21358. PMID: 17480015.
BibTeX
@article{quesada2007-17480015,
author = {Quesada, A. and Romeo, H. E. and Micevych, P.},
title = {{Distribution and localization patterns of estrogen receptor-beta and insulin-like growth factor-1 receptors in neurons and glial cells of the female rat substantia nigra: localization of ERbeta and IGF-1R in substantia nigra}},
journal = {The Journal of comparative neurology},
year = {2007},
doi = {10.1002/cne.21358},
pmid = {17480015},
url = {https://doi.org/10.1002/cne.21358}
}
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Key findings
- Stereological measurements revealed that 40% of the subpopulation of tyrosine hydroxylase-immunoreactive (TH-ir) SN pars compacta (SNpc) DA neurons are immunoreactive for estrogen receptor-beta (ERbeta).
- In situ hybridization and immunocytochemistry studies confirmed the expression of IGF-1R mRNA and revealed that almost all TH-ir SNpc DA neurons were immunoreactive for IGF-1R, respectively.
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Study details
- Evidence strengthLow
How this study scored 36/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomised / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 21 of the 58 points we could judge it on, which is 36 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (The Journal of comparative neurology) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2007 — within 20 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Laboratory or animal study (title names “rat”) — scores zero |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 17480015) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 21 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 21 of the 58 points we could judge it on is 36 out of 100. |
| Total | 36 / 100 | — |
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